p.23 抽出テキスト

.................................................................................................... levosimendan may restore RVpulmonary arterial coupling in acute PE by combining pulmonary vasodilation with an increase in RV contractility,242 no evidence of clinical benefit is available.

Vasodilators decrease PAP and PVR, but may worsen hypotension and systemic hypoperfusion due to their lack of specificity for the pulmonary vasculature after systemic [intravenous (i.v.)] administration. Although small clinical studies have suggested that inhalation of nitric oxide may improve the haemodynamic status and gas exchange of patients with PE,243245 no evidence for its clinical efficacy or safety is available to date.246

6.1.3 Mechanical circulatory support and oxygenation The temporary use of mechanical cardiopulmonary support, mostly with venoarterial extracorporeal membrane oxygenation (ECMO), may be helpful in patients with high-risk PE, and circulatory collapse or cardiac arrest. Survival of critically ill patients has been described in a number of case series,247252 but no RCTs testing the efficacy and safety of these devices in the setting of high-risk PE have been conducted to date. Use of ECMO is associated with a high incidence of complications, even when used for short periods, and the results depend on the experience of the centre as well as patient selection. The increased risk of bleeding related to the need for vascular access should be considered, particularly in patients undergoing thrombolysis. At present, the use of ECMO as a stand-alone technique with anticoagulation is controversial247,252 and additional therapies, such as surgical embolectomy, have to be considered.

A few cases suggesting good outcomes with use of the ImpellaV R catheter in patients in shock caused by acute PE have been reported.253,254

6.1.4 Advanced life support in cardiac arrest Acute PE is part of the differential diagnosis of cardiac arrest with non-shockable rhythm against a background of pulseless electrical activity. In cardiac arrest presumably caused by acute PE, current guidelines for advanced life support should be followed.255,256 The decision to treat for acute PE must be taken early, when a good outcome is still possible. Thrombolytic therapy should be considered; once a thrombolytic drug is administered, cardiopulmonary resuscitation should be continued for at least 6090 min before terminating resuscitation attempts.257

6.2 Initial anticoagulation

6.2.1 Parenteral anticoagulation In patients with high or intermediate clinical probability of PE (see section 4), anticoagulation should be initiated while awaiting the results of diagnostic tests. This is usually done with subcutaneous, weightadjusted low-molecular weight heparin (LMWH) or fondaparinux (Supplementary Data Table 5), or i.v. unfractionated heparin (UFH). Based on pharmacokinetic data (Supplementary Data Table 6),259 an equally rapid anticoagulant effect can also be achieved with a nonvitamin K antagonist oral anticoagulant (NOAC), and phase III clinical trials have demonstrated the non-inferior efficacy of a single-oral drug anticoagulation strategy using higher doses of apixaban for 7 days or rivaroxaban for 3 weeks.259261 LMWH and fondaparinux are preferred over UFH for initial anticoagulation in PE, as they carry a lower risk of inducing major bleeding and heparin-induced thrombocytopenia.262265 Neither LMWH nor fondaparinux need routine monitoring of anti-Xa levels. Use of UFH is nowadays largely restricted to patients with overt haemodynamic instability or imminent haemodynamic decompensation in whom primary reperfusion treatment will be necessary. UFH is also recommended for patients with serious renal impairment [creatinine clearance (CrCl) <_30 mL/min] or severe obesity. If LMWH is prescribed in patients with CrCl 15 - 30 mL/min, an adapted dosing scheme should be used. The

Table 9 Treatment of right ventricular failure in acute high-risk pulmonary embolism

Strategy Properties and use Caveats Volume optimization Cautious volume loading, saline, or Ringer’s lactate, <_500 mL over 1530 min Consider in patients with normallow central venous pressure (due, for example, to con-

comitant hypovolaemia) Volume loading can over-distend the RV, worsen ventricular interdependence, and reduce

CO239

Vasopressors and inotropes Norepinephrine, 0.21.0 mg/kg/mina 240 Increases RV inotropy and systemic BP, promotes positive ventricular interactions, and

restores coronary perfusion gradient Excessive vasoconstriction may worsen tissue perfusion

Dobutamine, 220 mg/kg/min241 Increases RV inotropy, lowers filling pressures May aggravate arterial hypotension if used

alone, without a vasopressor; may trigger or aggravate arrhythmias

Mechanical circulatory support Venoarterial ECMO/extracorporeal life support251,252,258 Rapid short-term support combined with

oxygenator Complications with use over longer periods

(>510 days), including bleeding and infections; no clinical benefit unless combined with surgical embolectomy; requires an experienced team

CO = cardiac output; BP = blood pressure; ECMO = extracorporeal membrane oxygenation; RV = right ventricle/ventricular. aEpinephrine is used in cardiac arrest. Downloaded from academic.oup.com/eurheartj/article/41/4/543/5556136 by guest on 07 October 2026